Target end organ disease among African Americans emphasizes the need for further investigation into the underlying pathophysiologic mechanisms of this desease process to more effectively determine treatment. We hypothesize that Candesartan Cilexitil, an angiotensin II receptor blocker will reduce vascular hypertrophy in hypertensives and therefore improve vascular supply to skeletal muscle, the primary site for insulin resistance (Study A). The change in vascular supply to the skeletal muscle will promote a further change in the architecture of the skeletal muscle fiber type. The result will be an increase in the fast twitch to slow twitch fiber ratio from baseline to the end of treatment and an overall improvement in insulin sensitivity at the skeletal muscle level and whole body metabolism ( Study B).